The aim of the proposed research is the determination of the aortic wall calcification potential in hypertension vis-a-vis normotension. Preliminary data indicate that once exposed to high blood pressure, the vascular wall is more susceptible to mineralization. This finding will be more extensively studied along with the time course of its development in relation to the development of hypertension. In addition, the effect of reversal of hypertension on the enhanced calcifiability will be monitored to determine if this pathology is itself reversible. The background for this proposal lies in the general finding that hypertension potentiates the development of further cardiovascular disease, and in the specific findings that hypertension (1) causes accumulation of elastic fiber and (2) results in fragmentation of the elastic lamina. These latter pieces of information are significant in that it has been shown that the elastic fiber is the initial site of arterial wall calcification and it is at breaks in this fiber that calcium phosphate is first laid down. Aortas from DOCA-NaCl rats, spontaneously hypertensive rats (SHR), and rats with coarctation hypertension and their appropriate controls will be tested for their ability to calcify in a serum calcifying medium. Extent of calcification as a function of time will be followed with scanning electron microscopy and electron probe microanalysis and by monitoring Ca-45 and P-32 uptake into the tissue. The degree to which this enhanced calcification impairs vessel wall resiliency will be determined by following its stress-strain characteristics as a function of the extent of its calcification. In addition, the calcification potential of connective tissue matrices elaborated by aortic smooth muscle cells grown in culture under conditions mimicing hypertension will be determined. The potential medical significance would be that this pathology could be related to hypertension's role as a risk factor in further cardiovascular disease, for example in atherosclerosis, to development of systolic hypertension, to accelerated aging of the vessel wall, to disadvantageous perfusion of the coronary arteries during diastole.